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Find studies

Showing 776–800 of 932 studies published 2026 · free to read (page 32 of 38) · 30,580 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

ADAM10 y su implicación en la enfermedad de Alzheimer

✓ Peer-reviewed alzhub usefulness score 27 out of 100. Neurología 2026-05-23

Resumen Introducción La vía amiloidogénica de procesamiento de la proteína precursora del amiloide es bien conocida a nivel de patogenia y terapéutica en la enfermedad de Alzheimer (EA), mientras que la vía no-amiloidogénica ha sido menos estudiada. 5 key findings →

Evidence: low

A Doença de Alzheimer (DA) é uma patologia neurodegenerativa de caráter progressivo, marcada pela deterioração gradual das funções cognitivas e motoras do indivíduo, com o consequente comprometimento da memória, da linguagem e do comportamento. 5 key findings →

Evidence: low

La aprobación de lecanemab y donanemab para el tratamiento de la enfermedad de Alzheimer temprana plantea nuevos desafíos para la neurología vascular, principalmente por la aparición de anomalías en las imágenes relacionadas con el amiloide (ARIA). 5 key findings →

Evidence: low

Alzheimer disease (AD) is a progressive neurodegenerative disease and the most common cause of dementia in the world, which has a gradual deterioration of memory, thinking and autonomy. 2 key findings →

Evidence: low

Alzheimer disease (AD) is the neurodegenerative condition that occurs in the elderly population above 65 years old and is the major cause of dementia. 5 key findings →

Evidence: low

Alzheimer's disease (AD) is a neurodegenerative disorder involving the amyloid-β plaque deposition, tau pathology, synaptic dysfunction, and impairment in cognition. 3 key findings →

Evidence: low

Alzheimer disease (AD) is a multi-factorial neurodegenerative disease that is characterized by accumulation of amyloid-beta (Aβ), protein aggregation and progressive neuronal dysfunction. 1 key finding →

Evidence: low

Các bệnh lý như lao và Alzheimer đòi hỏi phát hiện sớm với độ nhạy cao để can thiệp kịp thời, tuy nhiên các kỹ thuật hiện nay như ELISA, PCR còn hạn chế về chi phí và độ nhạy. Những tiến bộ gần đây trong công nghệ nano cho thấy hạt nano vàng vỏ đồng kết hợp sinh phẩm tái tổ hợp (protein hoặc aptamer) có thể khuếch đại tín hiệu màu, mở ra triển vọng cho chẩn đoán sớm siêu nhạy. Bài tổng quan này phân tích cơ chế kỹ thuật xét nghiệm kháng nguyên bằng sự hình thành vỏ nano đồng trên hạt vàng, trong đó ion Cu²⁺ được khử bởi natri ascorbate trên bề mặt AuNPs với vai trò ổn định của polyethylenimine, tạo cấu trúc Au-Cu đa giác giúp tăng cường tín hiệu plasmon. 5 key findings →

Evidence: low

Las enfermedades neurodegenerativas representan un importante problema de salud pública debido a su creciente prevalencia y al carácter progresivo e irreversible del daño neuronal que producen. 5 key findings →

Evidence: low

Esse artigo buscou abordar a Doença de Alzheimer de Início Precoce (DAIP) acerca do curso clínico, dos fatores predisponentes e do manejo, por meio de uma revisão de literatura, com ênfase na diferenciação entre DAIP e Doença de Alzheimer de Início Tardio (DAIT), incluindo artigos publicados entre 2015 e 2025, obtidos nas bases de dados “Alzheimer's Association”, “ScienceDirect”, “Cochrane” e “PubMed”, utilizando as palavras-chave “Alzheimer”, “early” e “on-set”, com o conectivo AND. 4 key findings →

Evidence: low

In 2026, the beginning of the 15th Five-Year Plan, the Central No. 1 Document emphasized the cultivation and expansion of county-level wealth-creating industries as the core approach to ensuring stable income growth for farmers. 5 key findings →

Evidence: low

Down syndrome postmortem brains exhibit reduction in [ 18 F]nifene binding to α4β2* nicotinic acetylcholinergic receptors

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-15

Alzheimer’s disease (AD) pathology including amyloid beta (Aβ) plaques and tau tangles accumulate with age in Down Syndrome (DS). 4 key findings →

Evidence: low

Oligodendrocyte Enriched Brain Organoids Reveal Impaired Oligodendroglial Maturation and Altered Neural Network Activity in Down Syndrome

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-08-28

Individuals with Down syndrome (DS) display developmental delay, intellectual disability, premature brain ageing, and an increased risk of Alzheimer-like neurodegeneration. 4 key findings →

Evidence: low

Alzheimer's disease progresses heterogeneously across diverse cohorts, yet current predictive models fail to capture this complexity while remaining clinically interpretable. 4 key findings →

Design: longitudinal study Participants: 1,669 Evidence: moderate

These aggregated proteins contribute to the pathological and clinical heterogeneity of AD and are associated with a more rapid progression. 4 key findings →

Participants: 1,304 Evidence: low

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Where “Free full text” comes from

Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled.

How the 0–100 score works — and why some entries are capped

This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.

  • Journal tier up to 10 pts
  • Journal's citation record up to 4 pts
  • Study design up to 12 pts
  • Strength of evidence up to 5 pts
  • Peer-review validation up to 10 pts
  • How recent up to 5 pts
  • Sample size up to 4 pts
  • Effect reported up to 3 pts
  • Studied in people up to 3 pts
  • Randomised / blinded up to 2 pts
  • Times cited up to 7 pts
  • Citations per year up to 5 pts
  • Impact for its field and year up to 6 pts
  • Cited by studies here up to 6 pts
  • Still being cited up to 4 pts
  • Senior author's track record up to 4 pts
  • Institution's track record up to 3 pts
  • Multi-centre collaboration up to 3 pts
  • Indexed in PubMed up to 2 pts
  • Free to read up to 2 pts

Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.

Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.

We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.

The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.

See the whole rubric drawn out → — four charts covering all 30,580 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.

What this library is — and isn't

This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.

1,037 records (3.4% of the library) are not peer-reviewed — 964 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.

See the full, machine-readable breakdown of this library's coverage →

Newest studies, as a dated timeline →    Atom feed    Where this research is being discussed: events